Masato Mizuashi, Tomoyuki Ohtani, Satoshi Nakagawa, Setsuya Aiba 

Slides:



Advertisements
Similar presentations
Proinflammatory cytokine–induced and chemical mediator–induced IL-8 expression in human bronchial epithelial cells through p38 mitogen-activated protein.
Advertisements

MicroRNA-21 Expression in CD4+ T Cells Is Regulated by STAT3 and Is Pathologically Involved in Sézary Syndrome  Leslie van der Fits, Marloes S. van Kester,
In situ Delivery of Tumor Antigen– and Adjuvant-Loaded Liposomes Boosts Antigen- Specific T-Cell Responses by Human Dermal Dendritic Cells  Martine A.
Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways  Rami Bechara, Diane Antonios,
Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways  Rami Bechara, Diane Antonios,
The CXC-chemokine platelet factor 4 promotes monocyte survival and induces monocyte differentiation into macrophages by Barbara Scheuerer, Martin Ernst,
CD271 on Melanoma Cell Is an IFN-γ-Inducible Immunosuppressive Factor that Mediates Downregulation of Melanoma Antigens  Junpei Furuta, Takashi Inozume,
Nonmetal Haptens Induce ATP Release from Keratinocytes through Opening of Pannexin Hemichannels by Reactive Oxygen Species  Kaoru Onami, Yutaka Kimura,
Sequential Polarization and Imprinting of Type 1 T Helper Lymphocytes by Interferon-γ and Interleukin-12  Edda G. Schulz, Luca Mariani, Andreas Radbruch,
Cord Blood CD34+ Cells Differentiate into Dermal Dendritic Cells in Co-Culture with Cutaneous Fibroblasts or Stromal Cells  Zia U.A. Mollah, Setsuya Aiba,
Oxidation of Cell Surface Thiol Groups by Contact Sensitizers Triggers the Maturation of Dendritic Cells  Saori Kagatani, Yoshinori Sasaki, Morihiko Hirota,
Phosphatidylinositol 3-Kinase/Akt-Dependent and -Independent Protection Against Apoptosis in Normal Human Melanocytes  Masahiro Oka, Akiko Kageyama, Mizuho.
Volume 63, Issue 3, Pages (March 2003)
Volume 68, Issue 4, Pages (October 2005)
Human Keratinocytes Express Functional CD14 and Toll-Like Receptor 4
IFNλ Stimulates MxA Production in Human Dermal Fibroblasts via a MAPK-Dependent STAT1-Independent Mechanism  Adewonuola A. Alase, Yasser M. El-Sherbiny,
Indomethacin Sensitizes TRAIL-Resistant Melanoma Cells to TRAIL-Induced Apoptosis through ROS-Mediated Upregulation of Death Receptor 5 and Downregulation.
Involvement of Oxidative Stress in Apoptosis Induced by a Mixture of Isothiazolinones in Normal Human Keratinocytes  Anna Ettorre, Paolo Neri, Anna Di.
Age-Related Differences in Sensitivity of Peripheral Blood Monocytes to Lipopolysaccharide and Staphylococcus Aureus Toxin B in Atopic Dermatitis  Marie.
Nonmetal Haptens Induce ATP Release from Keratinocytes through Opening of Pannexin Hemichannels by Reactive Oxygen Species  Kaoru Onami, Yutaka Kimura,
Norito Katoh, Fujiko Soga, Takeshi Nara, Koji Masuda, Saburo Kishimoto 
Phenotypic and Functional Outcome of Human Monocytes or Monocyte-Derived Dendritic Cells in a Dermal Equivalent  G. Guironnet, C. Dezutter-Dambuyant,
IL-10-Producing Langerhans Cells and Regulatory T Cells Are Responsible for Depressed Contact Hypersensitivity in Grafted Skin  Ryutaro Yoshiki, Kenji.
Marcel C. Pasch  Journal of Investigative Dermatology 
Macrophage Colony-stimulating Factor in Cooperation with Transforming Growth Factor- β1 Induces the Differentiation of CD34+ Hematopoietic Progenitor Cells.
IL-31 Induces Chemotaxis, Calcium Mobilization, Release of Reactive Oxygen Species, and CCL26 in Eosinophils, Which Are Capable to Release IL-31  Nikola.
Aggregation of the High-Affinity IgE Receptor FcεRI on Human Monocytes and Dendritic Cells Induces NF-κB Activation  Stefan Kraft, Natalija Novak, Thomas.
Targeting allergen to FcγRI reveals a novel TH2 regulatory pathway linked to thymic stromal lymphopoietin receptor  Kathryn E. Hulse, PhD, Amanda J. Reefer,
Poly(I:C)-Treated Human Langerhans Cells Promote the Differentiation of CD4+ T Cells Producing IFN-γ and IL-10  Laetitia Furio, Hermine Billard, Jenny.
Georg Varga, Nadine Nippe, Sandra Balkow, Thorsten Peters, Martin K
Skin CD4+ T Cells Produce Interferon-γIn Vitro in Response to Streptococcal Antigens in Chronic Plaque Psoriasis  Dean W. Brown, Barbara S. Baker, Jean-Marc.
Autocrine IL-21 Stimulation Is Involved in the Maintenance of Constitutive STAT3 Activation in Sézary Syndrome  Leslie van der Fits, Jacoba J. Out-Luiting,
Human Plasmacytoid Dendritic Cells Express Receptors for Anaphylatoxins C3a and C5a and Are Chemoattracted to C3a and C5a  Ralf Gutzmer, Brigitta Köther,
Leslie van der Fits, Jacoba J. Out-Luiting, Cornelis P
P38 Mitogen-activated Protein Kinase and Extracellular Signal-regulated Kinases Play Distinct Roles in the Activation of Dendritic Cells by Two Representative.
NKG2D Triggers Cytotoxicity in Murine Epidermal γδ T Cells via PI3K-Dependent, Syk/ZAP70-Independent Signaling Pathway  Atsuko Ibusuki, Kazuhiro Kawai,
P38 Mitogen-Activated Protein Kinase Mediates Dual Role of Ultraviolet B Radiation in Induction of Maturation and Apoptosis of Monocyte-Derived Dendritic.
Production and Pharmacologic Modulation of the Granulocyte-Associated Allergic Responses to Ovalbumin in Murine Skin Models Induced by Injecting Ovalbumin-
Activation and Translocation of p38 Mitogen-Activated Protein Kinase After Stimulation of Monocytes With Contact Sensitizers  Pia Brand, Sibylle Plochmann,
CX-659S, a Diaminouracil Derivative, Indirectly Inhibits the Function of Langerhans Cells by Blocking the MEK1/2-Erk1/2 Pathway in Keratinocytes  Hiroshi.
Human Keratinocytes Respond to Osmotic Stress by p38 Map Kinase Regulated Induction of HSP70 and HSP27  M. Garmyn, A. Pupe  Journal of Investigative Dermatology 
Maria C. Lebre, Angelic M. G. van der Aar, Lisa van Baarsen, Toni M. M
Resistance of Human Melanoma Cells Against the Death Ligand TRAIL Is Reversed by Ultraviolet-B Radiation via Downregulation of FLIP  Elke Zeise, Michael.
Yu-Ying He, Jian-Li Huang, Michelle L. Block, Jau-Shyong Hong, Colin F
Adenosine Receptors as Mediators of Both Cell Proliferation and Cell Death of Cultured Human Melanoma Cells  Stefania Merighi, Prisco Mirandola, Daniela.
Gang Li, Jason A. Bush, Vincent C. Ho 
Activation of Dual Apoptotic Pathways in Human Melanocytes and Protection by Survivin  Tong Liu, Diana Biddle, Adrianne N. Hanks, Brook Brouha, Hui Yan,
Human CD4+ T Lymphocytes with Remarkable Regulatory Functions on Dendritic Cells and Nickel-Specific Th1 Immune Responses  Andrea Cavani, Francesca Nasorri,
Dysregulation of Lymphocyte Interleukin-12 Receptor Expression in Sézary Syndrome  Mohamed H. Zaki, Ryan B. Shane, Yuemei Geng, Louise C. Showe, Suzanne.
Characterization of the Sensitizing Potential of Chemicals by In Vitro Analysis of Dendritic Cell Activation and Skin Penetration  Pierre Aeby, Christoph.
Regulatory T Cells from IL-10-Deficient Mice Fail to Suppress Contact Hypersensitivity Reactions Due to Lack of Adenosine Production  Sabine Ring, Alexander.
Human Beta-Defensin 3 Induces Maturation of Human Langerhans Cell–Like Dendritic Cells: An Antimicrobial Peptide that Functions as an Endogenous Adjuvant 
Solar-Simulated Ultraviolet Radiation Induces Abnormal Maturation and Defective Chemotaxis of Dendritic Cells  María Mittelbrunn, Reyes Tejedor, Hortensia.
Serotonin Activates Human Monocytes and Prevents Apoptosis
IL-4 and IL-13 Alter Plasmacytoid Dendritic Cell Responsiveness to CpG DNA and Herpes Simplex Virus-1  Jurjen Tel, Ruurd Torensma, Carl G. Figdor, I.
Double-Stranded RNA-Exposed Human Keratinocytes Promote Th1 Responses by Inducing a Type-1 Polarized Phenotype in Dendritic Cells: Role of Keratinocyte-Derived.
UVA-Induced Immune Suppression Through an Oxidative Pathway
High Calcium, ATP, and Poly(I:C) Augment the Immune Response to β-Glucan in Normal Human Epidermal Keratinocytes  Carren Sy Hau, Yayoi Tada, Sayaka Shibata,
Human Langerhans Cells Are More Efficient Than CD14−CD1c+ Dermal Dendritic Cells at Priming Naive CD4+ T Cells  Laetitia Furio, Isabelle Briotet, Alexandra.
Induction of RANTES by TWEAK/Fn14 Interaction in Human Keratinocytes
Formation of Antigenic Quinolone Photoadducts on Langerhans Cells Initiates Photoallergy to Systemically Administered Quinolone in Mice  Akihiro Ohshima,
Jennifer G. Georgiou, Kristen K. Skarratt, Stephen J
Tumor Necrosis Factor-α- and IL-4-Independent Development of Langerhans Cell-Like Dendritic Cells from M-CSF-Conditioned Precursors  Jean-Baptiste Barbaroux,
Tomoyuki Ohtani, Setsuya Aiba, Masato Mizuashi, Zia U. A
Interleukin-3 in Cooperation with Transforming Growth Factor β Induces Granulocyte Macrophage Colony Stimulating Factor Independent Differentiation of.
Thiol Antioxidants Block the Activation of Antigen-Presenting Cells by Contact Sensitizers  Stefanie Bruchhausen, Sabine Zahn, Elke Valk, Jürgen Knop,
Volume 61, Issue 2, Pages (February 2002)
Coupling of Contact Sensitizers to Thiol Groups is a Key Event for the Activation of Monocytes and Monocyte-Derived Dendritic Cells  Detlef Becker, Elke.
Roland Houben, Sonja Ortmann, Astrid Drasche, Jakob Troppmair, Marco J
Interleukin-17 is Produced by Both Th1 and Th2 Lymphocytes, and Modulates Interferon-γ- and Interleukin-4-Induced Activation of Human Keratinocytes  Cristina.
Presentation transcript:

Redox Imbalance Induced by Contact Sensitizers Triggers the Maturation of Dendritic Cells  Masato Mizuashi, Tomoyuki Ohtani, Satoshi Nakagawa, Setsuya Aiba  Journal of Investigative Dermatology  Volume 124, Issue 3, Pages 579-586 (March 2005) DOI: 10.1111/j.0022-202X.2005.23624.x Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Concentration of simple chemicals to induce cell death of monocyte-derived dendritic cells (MoDC). MoDC were treated with various concentrations of contact sensitizers or non-sensitizers for 24 h. Then the total percentage of both apoptotic cells (annexin V (+)) and necrotic cells (propidium iodide (PI) (+)) was assessed by flow cytometry. The mean±SEM of the percentage of annexin V-positive cells or PI-positive cells from seven independent experiments is shown. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and non-treated cells. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Some contact sensitizers at sublethal concentrations upregulated the expression of CD86 in monocyte-derived dendritic cells (MoDC). MoDC were either unstimulated or stimulated with sublethal concentrations of contact sensitizers, NiCl2, MnCl2, 2,4-dinitrochlorobenzene (DNCB), HCHO, and thimerosal, or non-sensitizers, ZnCl2, SDS, and benzalkonium chloride (BC) for 48 h. The surface expression of CD86 antigen was analyzed by flow cytometry. The mean±SEM of the relative mean fluorescence intensities (MFI) was determined from four to six independent experiments. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and relevant control cells, non-treated, or those treated with dimethyl sulfoxide (DMSO). Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 2,4-dinitrochlorobenzene (DNCB) and NiCl2 reduced the reduced/oxidized glutathione (GSH/GSSG) ratio in monocyte-derived dendritic cells (MoDC) at different kinetics. MoDC were cultured with 300 μM or 1 mM of NiCl2 or 10 or 30 μM of DNCB for 0, 1, 3, 10, 30, 60, and 120 min. After stimulation with the chemicals, the GSH/GSSG ratio in MoDC was assessed using colorimetric assays by the GSH reductase-DTNB recycling procedure. The relative GSH/GSSG ratio was calculated by the following formula. The relative GSH/GSSG=the GSH/GSSG ratio in MoDC treated with chemicals/that in non-treated MoDC. The mean±SEM of the relative GSH/GSSG ratio from three independent experiments is shown. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and the non-treated control. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 All contact sensitizers, but not non-sensitizers, at sublethal concentrations decreased the reduced/oxidized glutathione (GSH/GSSG) ratio in monocyte-derived dendritic cells (MoDC). MoDC were either unstimulated or stimulated with three concentrations of contact sensitizers, NiCl2, MnCl2, 2,4-dinitrochlorobenzene (DNCB), HCHO, and thimerosal, or non-sensitizers, ZnCl2, SDS, and benzalkonium chloride (BC) for 2 h. The three concentrations of each chemical consisted of a lethal concentration, sublethal concentration, and 1/3 of the sublethal concentration. Intracellular GSH and GSSG were measured using colorimetric assays by the GSH reductase-DTNB recycling procedure. The relative GSH/GSSG ratio was calculated as described in Materials and Methods. Each dot corresponds to the ratio obtained from different experiments and the mean±SEM of the relative GSH/GSSG ratio is also presented. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and the non-treated control. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 5 Contact sensitizers phosphorylated p38 mitogen-activated protein kinase (MAPK) in monocyte-derived dendritic cells (MoDC). MoDC were either unstimulated or stimulated with sublethal or lethal concentrations of contact sensitizers, NiCl2, 2,4-dinitrochlorobenzene (DNCB) HCHO, thimerosal, or non-sensitizer, benzalkonium chloride (BC), or sodium dodecyl sulfate (SDS) for different time periods, and the phosphorylation of p38 MAPK was analyzed by flow cytometry. Representative flow cytometry from three independent experiments 60 min after chemical stimulation is shown in (a). The time course of phosphorylation of p38 MAPK after stimulation of NiCl2 or DNCB and that after stimulation of HCHO, thimerosal, BC, or SDS is shown in (b) and (c), respectively. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and the non-treated control. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 6 N-acetyl-L-cysteine (NAC) increased the reduced/oxidized glutathione (GSH/GSSG) ratio in monocyte-derived dendritic cells (MoDC) with or without chemical stimulation. To examine the effects of the antioxidant NAC, we added 25 mM NAC to the culture of MoDC 30 min prior to stimulation by the chemicals. Two hours after culture, the relative GSH/GSSG ratio of MoDC was calculated as described in Materials and Methods. The mean±SEM of the relative GSH/GSSG ratio from three to seven independent experiments is shown. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between MoDC treated with NAC and those untreated with NAC. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 7 N-acetyl-L-cysteine (NAC) suppressed the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in monocyte-derived dendritic cells (MoDC) stimulated with the contact sensitizers. MoDC were pretreated with 25 mM NAC for 30 min and then cultured with 300 μM or 1 mM of NiCl2 (a) or 10 or 30 μM of 2,4-dinitrochlorobenzene (DNCB) (b). After 0–60 min of culture, the phosphorylation of p38 MAPK was analyzed by flow cytometry. The relative GSH/GSSG ratio was calculated as described in Materials and Methods. This is a representative flow cytometry of two independent experiments. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 8 N-acetyl-L-cysteine (NAC) suppressed the augmentation of CD86 expression in monocyte-derived dendritic cells (MoDC) stimulated with the contact sensitizers. MoDC were pretreated with 25 mM NAC for 30 min and then cultured with or without 300 μM of NiCl2, 10 μM of 2,4-dinitrochlorobenzene (DNCB), 1 × 10-3% benzalkonium chloride (BC), or 0.01% dimethyl sulfoxide (DMSO). After 2 d of culture, their surface expression of CD86 was analyzed by flow cytometry. The histogram of chemical-treated MoDC in the absence or the presence of 25 mM NAC is expressed as a thick solid line or a solid line, whereas a shaded line or a dotted line indicates the histogram of non-treated dendritic cell (DC) or that of DC stained with an isotype control antibody, respectively. This is a representative flow cytometry of three independent experiments. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 9 Most contact sensitizers, but not non-sensitizers, at sublethal concentrations lowered the reduced/oxidized glutathione (GSH/GSSG) ratio in human monocytic cell-lineTHP-1 cells, and the effect that was abrogated by N-acetyl-L-cysteine (NAC). Human monocytic cell-line THP-1 cells were either unstimulated or stimulated with three concentrations of contact sensitizers, NiCl2, 2,4-dinitrochlorobenzene (DNCB), HCHO, and thimerosal, or non-sensitizers, SDS and benzalkonium chloride (BC) for 2 h, and then, the GSH/GSSG ratio was measured by the same procedure as shown in Figure 4. At sublethal concentrations, all contact sensitizers except for HCHO, but none of the non-sensitizers, lowered the GSH/GSSG ratio in THP-1 cells. The means±SEM of the GSH/GSSG ratio was determined in five independent experiments. Asterisks indicate significance (**p<0.01, *p<0.05) for the difference between stimulated cells and the non-treated control. Journal of Investigative Dermatology 2005 124, 579-586DOI: (10.1111/j.0022-202X.2005.23624.x) Copyright © 2005 The Society for Investigative Dermatology, Inc Terms and Conditions